Therefore, a model where Abi1 and Cortactin act cooperatively in invadopodia at the leading edge of colorectal carcinoma is quite conceivable; phosphorylated Abi1 would then support local actin reorganization via activation of nucleation-promoting factors, giving rise to a branched actin network required for ECM attachment and invadopodia formation (schematically depicted in Figure 5) [4,16]. The gene discussed is CTTN; the disease is colorectal carcinoma.